Fig. 2

LPS-induced systemic inflammation induced the programmed necroptosis pathway and Kir4.1 dysregulation in the hippocampus. Three days after LPS or vehicle (saline) injection, 3 mg/kg kainic acid or vehicle (saline) was intraperitoneally administrated to the mice. Two hours later, the hippocampus was obtained for assessing the protein expression (n = 3 per group) using Western blots. A A representative Western blot images showing the specific bands for these proteins. An equal amount of protein sample (30 μg) obtained from the hippocampus homogenate was applied to each lane, and α-tubulin protein was used as an internal control. B–D Bar graph showing the densitometric analysis of the molecules JNK, Bax, and cCaspase 3 involved in the apoptotic pathway; E–G of the proteins phosphated RIP3, phosphated MLKL, and TNFα in the necroptosis pathway; and (H and I) of the proteins NCKK1 and Kir4.1 in ion channels, normalized to α-tubulin expression. Each bar represents the mean ± SEM. One-way ANOVA; Bonferroni post hoc test among the groups; *p < 0.05, **p < 0.01, and ***p < 0.001